Weapons of STAT destruction - Interferon evasion by paramyxovirus V proteins

被引:135
作者
Horvath, CM
机构
[1] Northwestern Univ, Dept Biochem Mol Biol & Cell Biol, Evanston, IL 60208 USA
[2] Northwestern Univ, Dept Med, Evanston, IL 60208 USA
[3] Northwestern Univ, Evanston NW Healthcare Res Inst, Dept Med, Evanston, IL 60208 USA
来源
EUROPEAN JOURNAL OF BIOCHEMISTRY | 2004年 / 271卷 / 23-24期
关键词
antiviral; interferon; paramyxovirus; STAT; viral evasion;
D O I
10.1111/j.1432-1033.2004.04425.x
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The signal transducer and activator of transcription (STAT) family of proteins function to activate gene transcription downstream of myriad cytokine and growth factor signals. The prototype STAT proteins, STAT1 and STAT2, are required for innate and adaptive antimicrobial immune responses that result from interferon signal transduction. While many viruses have evolved the ability to avoid these antiviral cytokines, the Paramyxoviruses are distinct in their abilities to interfere directly with STAT proteins. Individual paramyxovirus species differ greatly in their precise mechanism of STAT signaling evasion, but a virus-encoded protein called V plays a central role in this process. The theme of V-dependent interferon evasion and its variations provide significant insights into virus-host interactions and viral immune evasion that can help define targets for antiviral drug design. Exposure of the viral weapons of STAT destruction may also be instructive for application to STAT-directed therapeutics for diseases characterized by STAT hyperactivity.
引用
收藏
页码:4621 / 4628
页数:8
相关论文
共 68 条
[61]   Paramyxoviruses SV5 and HPIV2 assemble STAT protein ubiquitin ligase complexes from cellular components [J].
Ulane, CM ;
Horvath, CM .
VIROLOGY, 2002, 304 (02) :160-166
[62]   Toll-like receptors and innate antiviral responses [J].
Vaidya, SA ;
Cheng, GH .
CURRENT OPINION IN IMMUNOLOGY, 2003, 15 (04) :402-407
[63]   Molecular biology of Hendra and Nipah viruses [J].
Wang, LF ;
Harcourt, BH ;
Yu, M ;
Tamin, A ;
Rota, PA ;
Bellini, WJ ;
Eaton, BT .
MICROBES AND INFECTION, 2001, 3 (04) :279-287
[64]   Naturally occurring substitutions in the P/V gene convert the noncytopathic paramyxovirus simian virus 5 into a virus that induces alpha/beta interferon synthesis and cell death [J].
Wansley, EK ;
Parks, GD .
JOURNAL OF VIROLOGY, 2002, 76 (20) :10109-10121
[65]   C-terminal region of STAT-1α is not necessary for its ubiquitination and degradation caused by mumps virus V protein [J].
Yokosawa, N ;
Yokota, S ;
Kubota, T ;
Fujii, N .
JOURNAL OF VIROLOGY, 2002, 76 (24) :12683-12690
[66]   Measles virus suppresses interferon-α signaling pathway:: suppression of Jak1 phosphorylation and association of viral accessory proteins, C and V, with interferon-α receptor complex [J].
Yokota, S ;
Saito, H ;
Kubota, T ;
Yokosawa, N ;
Amano, K ;
Fujii, N .
VIROLOGY, 2003, 306 (01) :135-146
[67]   Paramyxoviridae use distinct virus-specific mechanisms to circumvent the interferon response [J].
Young, DF ;
Didcock, L ;
Goodbourn, S ;
Randall, RE .
VIROLOGY, 2000, 269 (02) :383-390
[68]   Single amino acid substitution in the V protein of simian virus 5 differentiates its ability to block interferon signaling in human and murine cells [J].
Young, DF ;
Chatziandreou, N ;
He, B ;
Goodbourn, S ;
Lamb, RA ;
Randall, RE .
JOURNAL OF VIROLOGY, 2001, 75 (07) :3363-3370